Heat transfer pathways between fetal lamb and ewe

Gilbert, R. D.; Schröder, H.; Kawamura, Tsunehiro; Dale, P.; Power, Gordon G.

doi:10.1152/jappl.1985.59.2.634

Cited by 55 publications

(40 citation statements)

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“…One possibility is that the carotid rete, which in the sheep helps cool the brain after birth (1), might remove heat from arterial blood supplying the brain. This seems unlikely, however, because before birth there is no effective sink into which heat might be deposited; the amniotic fluid is only 0.1-0.2°C cooler than fetal core temperature, and thus the temperature gradient for heat flux from the rete is small (18). Alternatively, a larger fraction of carotid flow perfusing non-brain tissues such as the face and scalp might be diverted to the brain during severe hypoxia than was evident from carotid blood flow measurements.…”

Section: Discussionmentioning

confidence: 99%

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Roelfsema¹,

Dean²,

Wassink³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The preterm fetus is capable of surviving prolonged periods of severe hypoxia without neural injury for much longer than at term. To evaluate the hypothesis that regulated suppression of brain metabolism contributes to this remarkable tolerance, we assessed changes in the redox state of cytochrome oxidase (CytOx) relative to cerebral heat production, and cytotoxic edema measured using cerebral impedance, during 25 min of complete umbilical cord occlusion or sham occlusion in fetal sheep at 0.7 gestation. Occlusion was followed by rapid, profound reduction in relative cerebral oxygenation and EEG intensity and an immediate increase in oxidized CytOx, indicating a reduction in electron flow down the mitochondrial electron transfer chain. Confirming rapid suppression of cerebral metabolism there was a loss of the temperature difference between parietal cortex and body at a time when carotid blood flow was maintained at control values. As occlusion continued, severe hypotension/hypoperfusion developed, with a further increase in CytOx levels to a plateau between 8 and 13 min and a progressive rise in cerebral impedance. In conclusion, these data strongly suggest active regulation of cerebral metabolism during the initial response to severe hypoxia, which may help to protect the immature brain from injury. asphyxia; preterm; umbilical cord occlusion FETAL AND NEONATAL ANIMALS are well known to be able to survive much longer periods of hypoxia than adults (9, 22). More recently, it has become clear that preterm animals can withstand even longer periods of profound hypoxia and hypotension/hypoperfusion without neural injury than at term (17,28,35). In part, this remarkable tolerance to hypoxia may be related to greater anaerobic capacity in the immature brain (48), but an important additional factor is likely to be actively regulated suppression of cerebral activity. This mechanism, which is mediated by release of endogenous inhibitory neuromodulators such as ␥-aminobutyric acid (GABA) and adenosine during hypoxia, recently has been shown to be active in near-term (0.8 to 0.9 gestation) fetal sheep (6,23,33,49). For example, hypoxemia or adenosine infusion in near-term fetal sheep increased oxidation of cerebral cytochrome oxidase (CytOx) on near-infrared measurements, indicating a rapid reduction in electron flow down the mitochondrial electron transfer chain and, thus, a fall in metabolic activity (40, 41). Conversely, blockade of adenosine A 1 receptor activity during umbilical cord occlusion in near-term fetal sheep accelerated the onset and increased the magnitude of cerebral anoxic cytotoxic edema, with subsequently increased neuronal loss (23).This regulated suppression of metabolic rate during hypoxia or ischemia, before energy stores are depleted, has been termed adaptive hypometabolism (38). It may be of considerable importance not only before birth but also during birth itself and in other settings involving adaptation to low oxygen levels (34). The near-term fetus of the high-altitude, hypoxia-adapted llama...

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Section: Discussionmentioning

confidence: 99%

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Roelfsema¹,

Dean²,

Wassink³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, these results suggest that body temperature measurement is useful for predicting impending parturition in this species. In vivo studies [13] and model predictions [14] have indicated that fetal lambs lose 80 to 85% of their heat via transfer to the placenta and the other 15 to 20% via transfer through the uterine wall. Blood flow to the placenta, was directly affected by maternal temperature, and this effect would influence heat dissipation by the fetus [14].…”

Section: Discussionmentioning

confidence: 99%

Body Temperature and Circulating Progesterone Levels before and after Parturition in Killer Whales (Orcinus orca)

et al. 2006

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Abstract. Killer whales were used to evaluate peripartum changes and interactions between body temperature and circulating progesterone concentration. Daily body temperature was measured between 0800 h and 0830 h before activity. Body temperature clearly increased during the first phase of pregnancy, and this was followed by a gradual decline until full term. The initial increase was paralleled by circulating levels of progesterone. A decrease in body temperature was first detected on day 5 (p<0.01) before parturition, and body temperature decreased significantly every 2 days until delivery. Five days before delivery, body temperature was 0.3 C lower than the mean value during the pregnancy period, and the decrease was more marked on day 1 before delivery (0.8 C). Serum progesterone levels during pregnancy showed a general pattern of initial rapid elevation (increasing phase), followed by a gradual decline (decreasing phase) throughout the remainder of pregnancy. However, statistically significant correlations between body temperature and progesterone pattern were only found only during the increasing phase. These results suggest that monitoring body temperature variation can be considered valuable for predicting impending parturition in killer whales.

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“…The contribution of the placental heat production to the fetal-maternal temperature difference has been estimated to be 0-07°C (Schr6der, Gilbert & Power, 1988). Estimates of both conductances have been obtained in fetal sheep (Gilbert, Schroder, Kawamura, Dale & Power, 1985) by observing fetal and amniotic fluid temperatures after injection of cold saline into the amniotic cavity. On (Schroder et al 1988) that changes of fetal heat production (oxygen consumption) and cardiac output (umbilical blood flow) will indeed influence fetal temperature, but the effects of fetal thermoregulatory efforts are very limited.…”

Section: Placental Heat Exchangementioning

confidence: 99%

Engine and radiator: fetal and placental interactions for heat dissipation

Schröder¹,

Power²

1997

Experimental Physiology

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SUMMARYThe 'engine' of fetal metabolism generates heat (3-4 W kg-' in fetal sheep) which has to be dissipated to the maternal organism. Fetal heat may move through the amniotic/allantoic fluids to the uterine wall (conductive pathway; total conductance, 1-1 W 0C-' kg-') and with the umbilical arterial blood flow (convective pathway) to the placenta. Because resistance to heat flow is larger than zero fetal temperature exceeds maternal temperature by about 0 5°C (0.3-1°C). Probably 85 % of fetal heat is lost to the maternal organism through the placenta, which thus serves as the main 'radiator'. Placental heat conductivity appears to be extremely high and this may lead to impaired heat exchange (guinea-pig placenta). A computer simulation demonstrates that fetal temperature is essentially clamped to maternal temperature, and that fetal thermoregulatory efforts to gain thermal independence would be futile. Indeed, when the late gestational fetus in uter^o is challenged by cold stress, direct and indirect indicators of (non-shivering) thermogenesis (oxygen consumption, increase of plasma glycerol and free fatty acid levels) change only moderately. In prematurely delivered lambs, however, cold stress provokes summit metabolism and maximum heat production. Only when birth is imitated in utero (by cord clamping, external artificial lung ventilation and cooling) do thermogenic efforts approach levels typical of extra-uterine life. This suggests the presence of inhibitors of thermogenesis of placental origin, e.g. prostaglandins and adenosine. When the synthesis of prostaglandins is blocked by pretreatment with indomethacin, sheep fetuses react to intra-uterine cooling with vigorous thermogenic responses, which can be subdued by infusion of prostaglandin E2 (PGE2). Since the sheep placenta is known to produce sufficient amounts of PGE2, it seems that the placenta controls fetal thermogenic responses to some extent. This transforms the fetus into an ectothermic organism, and yet allows the newborn the full exploitation of thermoregulatory responses typical of endothermic animals.

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Heat transfer pathways between fetal lamb and ewe

Cited by 55 publications

References 0 publications

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Body Temperature and Circulating Progesterone Levels before and after Parturition in Killer Whales (Orcinus orca)

Engine and radiator: fetal and placental interactions for heat dissipation

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